1/27. Fatal hepatic failure caused by chemotherapy-induced reactivation of hepatitis B virus in a patient with hematologic malignancy.A patient with hematologic malignancy and hepatitis b virus (HBV) infection received chemotherapy containing a glucocorticoid. The patient developed severe hepatitis after chemotherapy and, despite achieving complete remission of the malignancy, died of hepatic failure. We carried out a retrospective study of changes in the serological markers of HBV in this patient. Both serum hepatitis B surface antigen (HBsAg) and hepatitis B surface antibody (HBsAb) were negative on admission. During the course of chemotherapy, HBsAg gradually became positive, but no liver dysfunction was apparent until after completion of the chemotherapy. The patient showed no initial evidence of being a latent HBV carrier. Therefore, we believe that screening for HBsAg is insufficient for detecting latent HBV carriers, and that investigation for hepatitis B core antibody (HBcAb) is essential.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
2/27. lamivudine therapy for a hepatitis B surface antigen (HBsAg)-positive leukemia patient receiving myeloablative chemotherapy and autologous stem cell transplantation.hepatitis b virus (HBV) can be a cause of fatal liver failure after chemotherapy for viral carrier patients and limits the indication of myeloablative therapy for them. We describe an HBsAg-positive leukemia patient who successfully underwent autologous PBSC transplant. After chemotherapeutic treatment his serum HBV dna level rose in association with hepatitis. To prevent progression to fulminant hepatitis, we administered lamivudine, a viral reverse transcriptase inhibitor, during the transplantation procedure. The patient did not show any increase of HBV dna or a worsening of his hepatitis. Thus, lamivudine may be a promising treatment for HBsAg-positive patients receiving myeloablative chemotherapy and autologous stem cell transplantation.- - - - - - - - - - ranking = 4keywords = antigen (Clic here for more details about this article) |
3/27. Fulminant hepatitis type B after chemotherapy in a serologically negative hepatitis b virus carrier with acute myelogenous leukemia.We report a case of a 41-year-old man with acute myelogenous leukemia who developed fulminant hepatitis from reactivation of trace hepatitis b virus (HBV) 2 months after complete remission. Although he became positive for HB surface antigen at the onset of fulminant hepatitis, he had been negative for HBV serum markers, and only HBV dna was detected by polymerase chain reaction (PCR) amplification on admission. The original stocks of serum samples from all blood donors were tested again for HBV dna by PCR, and all samples were negative. This case demonstrates that testing for HBV dna by PCR is necessary before chemotherapy, because silent HBV carriers are rare and fulminant hepatitis may be induced by chemotherapy in patients with hematologic malignancies.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
4/27. Efficacy of lamivudine for the treatment of hepatitis b virus infection after liver transplantation in children.BACKGROUND: There is at present very little information about hepatitis b virus (HBV) infection in children after liver transplantation. This is the first study to assess the safety and efficacy of lamivudine in this patient population. methods: We describe three children aged 5-14 years who underwent liver transplantation for fulminant hepatitis a, hyperoxaluria, and cystic fibrosis. Despite adequate immunoprophylaxis, two of the children who were serum hepatitis B surface antigen-positive before transplantation (HBV dna-negative by hybridization) had a reactivation of the disease, and one had a de novo HBV infection, at 12-18 months after transplantation. lamivudine 3 mg/kg was administered on a compassionate-use basis for 14-36 months. RESULTS: After 1 month of therapy, HBV dna disappeared from the serum in all patients by hybridization and in two patients by polymerase chain reaction. In all three children, alanine transaminase levels normalized. One child developed lamivudine resistance after 22 months with no evidence of hepatic decompensation. Repeated liver histological studies revealed progression of hepatic fibrosis in one child. All children remained serum hepatitis B surface antigen- and hepatitis B e antigen-positive. No adverse effects of the drug were noted. CONCLUSION: lamivudine is beneficial and well tolerated in children with HBV infection after liver transplantation.- - - - - - - - - - ranking = 3keywords = antigen (Clic here for more details about this article) |
5/27. hepatitis b virus reactivation in a patient with chronic GVHD after allogeneic peripheral blood stem cell transplantation.We report a patient with fatal hepatitis b virus (HBV) reactivation after treatment for chronic graft-versus-host disease (GVHD) following allogeneic peripheral blood stem cell transplantation to treat chronic myelogenous leukemia. The presence of antibodies to hepatitis B surface antigen (HBsAb) prior to transplantation indicated previous HBV infection. Liver damage first developed 8 months after transplantation with the disappearance of HBsAb. Hepatitis B antigen was first noted during an examination of liver damage that occurred 22 months after transplantation. Retrospective examination of serum by real-time detection polymerase chain reaction (RTD-PCR) revealed HBV in both the first and second episodes of liver damage (89 copies/mL and 2 x 10(6) copies/mL, respectively). HBV may have been reactivated, leading to fatal liver damage in this HBsAb-positive patient. We propose that RTD-PCR-based analysis should be performed to diagnose liver dysfunction after hematopoietic stem cell transplantation.- - - - - - - - - - ranking = 2keywords = antigen (Clic here for more details about this article) |
6/27. Hepatic failure due to CD3 plasma cell infiltration of the liver in multiple myeloma.We present a case of multiple myeloma who died of liver failure 7.5 months after initial diagnosis. Postmortem liver biopsy revealed diffuse CD3-expressing plasma cell infiltration and eosinophilic amorphous material deposition which was considered as light chain deposits. T cell receptor-gamma rearrangement was not detected in liver biopsy sections using the polymerase chain reaction despite CD3 positivity. To our knowledge, this is the first report of CD3-expressing plasma cell infiltration in tissue sections. The discordance between the phenotype and the genotype suggests a partial activation of genes encoding the T cell antigens by the transforming event. We also concluded that CD3 positivity was associated with short survival, which is consistent with previous data.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
7/27. Fatal hepatic failure after emergence of the hepatitis b virus mutant during lamivudine therapy in a patient with liver cirrhosis.lamivudine therapy for chronic hepatitis and decompensated liver cirrhosis related to the hepatitis b virus (HBV) resulted in improvement of liver function and inhibition of viral replication. Despite emergence of the HBV mutant, e-antigen seroconversion and improvement of liver function may be achieved with continuation of lamivudine therapy. Although hepatic decompensation has been reported in a few cases after the emergence of lamivudine-resistant mutants, fatal cases of non-transplant patients have only rarely been reported in the literature. Here, we describe a patient with HBV-related liver cirrhosis who died after a breakthrough infection with a lamivudine-resistant mutant. Hepatic failure and mortality developed after flare-up of severe hepatitis after 13 months of lamivudine treatment. Emergence of the HBV mutant with substitution of isoleucine for leucine at residue 426 (L4261) in combination with isoleucine for methionine at residue 550 (M5501) was observed at 10 and 13 months of treatment.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
8/27. False findings of low protein C activity in two children with budd-chiari syndrome and factor v Leiden mutation.Two pediatric patients with budd-chiari syndrome are reported, who were heterozygous for factor v Leiden mutation. The first patient was falsely diagnosed with type II protein c deficiency, and the second was initially found to have decreased protein C activity based on a protein C clotting assay. Retesting by protein C chromogenic assay indicated that protein C activity was normal in both children. In patients with budd-chiari syndrome, low levels of protein C antigen and activity should be interpreted with caution, and within the context of factor v Leiden mutation status, parents' results, severity of liver dysfunction, and the type of protein C assay performed in order to avoid misdiagnosing protein c deficiency.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
9/27. lamivudine and Famciclovir resistant hepatitis b virus associated with fatal hepatic failure.BACKGROUND: lamivudine (LMV) is the only nucleoside analogue approved for the treatment of chronic hepatitis B (CHB). LMV, as with other nucleoside analogues including Famciclovir (FCV), suppresses the replication of hepatitis b virus (HBV) by targeting the viral polymerase. However, prolonged antiviral therapy results in the emergence of drug resistance HBV which can contribute to virological breakthroughs and recurrent hepatitis flares. OBJECTIVES: A 38-year-old hepatitis B e antigen (HBeAg) positive Chinese female infected with genotype B HBV commenced treatment with FCV and LMV combination therapy but was later maintained on LMV monotherapy. The patient remained HBeAg positive throughout treatment. Virological breakthrough occurred with the emergence of drug resistant HBV. This coincided with worsening liver function and the patient died of subacute fulminant hepatitis. This study evaluated the virological factors that contributed to the clinical decline of the patient. STUDY DESIGN: Biochemical analysis and full-length HBV genomic sequencing were performed on serial serum samples collected from the patient before and during antiviral therapy. RESULTS: Virological analysis revealed that the pre-treatment dominant HBV quasispecies in the patient had a number of non-consensus genotype B mutations which were located in the basal core promoter (BCP), polymerase, X, core and S genes. Subsequent to the instigation of antiviral therapy, the dominant drug resistant HBV which caused virological breakthrough and was associated with hepatic failure displayed a series of unique mutations particularly in the BCP (A1762T and G1764A) and in the polymerase (rtL180M, rtM204V, rtA222T and rtL336V), core (cP5T, cS26A, cV85I and cP135A), surface (sI195M and sM213I) and X (xK95Q, xN118T, xK130M and xV131I) proteins. CONCLUSIONS: Monitoring for the accumulation of unique mutations within the genome of drug resistant HBV mutants isolated during long term antiviral therapy appears warranted in the clinical management of patients with CHB.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
10/27. Fulminant hepatitis after infliximab in a patient with hepatitis b virus treated for an adult onset still's disease.Infliximab, a chimeric anti-tumor necrosis factor-alpha monoclonal antibody, has been demonstrated to be efficient and safe in patients with active rheumatoid arthritis and in the management of severe bouts of Crohn's disease. However, the safety of infliximab has not been evaluated in patients infected with hepatitis b virus. We report the case of a 28-year-old woman, with a positive hepatitis b virus surface antigen, who developed fulminant hepatitis 2 weeks after receiving a second infliximab infusion for a refractory adult onset Still's disease.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
| | Next -> |